Prediction and Effect of Maternal Marginal Zinc Deficiency on Development, Redox Status, and Gene Expression Related to Oxidation and Apoptosis of Embryos

Abstract

BackgroundMaternal severe zinc (Zn) deficiency induced oxidative damage and apoptosis in embryos, resulting in growth retardation. Therefore, it is crucial to assess maternal marginal Zn nutritional status for poultry breeders to prevent embryos subjected to severe Zn deficiency. MethodsIn Exp. 1, twelve egg embryos were sampled at incubation day 17 (E17), E20, E23, E26, E29, and E32 (day of hatch) respectively, with 6 replicates of 2 embryo each. The developmental changes of Zn mobilization and Zn transport gene mRNA expression were determined. In Exp. 2, 324 laying duck breeders were randomly allotted into 3 dietary Zn levels (0, 60, and 120 mg Zn/kg diet) with 6 replicates of 18 ducks per replicate. Plasma Zn concentration and erythrocytic Zn metalloenzyme activities in breeders as well as the development, redox status, and gene expression related to oxidation and apoptosis in embryos were measured. Blood samples were collected at the 2th, 4th and 6th weeks of the experiment. ResultsIn Exp. 1, the overall Zn mobilization rates were increased in yolk sac and embryonic liver in response to the increased incubation period, associated with the decreased ZIP10, 13, and 14 mRNA expressions in embryonic liver (P < 0.05). In Exp. 2, with the prolonged dietary Zn depletion, maternal Zn deficiency decreased plasma Zn concentration and erythrocytic alkaline phosphatase activity at the 6th week and inhibited erythrocytic 5'-nucleotidase (5’-NT) activity at 2th week (P < 0.05). On E29 of the maximal rate of Zn mobilization, maternal marginal Zn deficiency increased middle and late embryonic mortality and contents of superoxide anion radical, MDA and PPC, as well as decreasedMT content, CuZnSOD activity, and MT1 mRNA expression in embryonic livers (P < 0.05). Additionally, maternal marginal Zn deficiency increased BCL2-associated X protein and Caspase-9 mRNA expression and decreased B-cell lymphoma-2 mRNA expression in embryonic liver (P < 0.05). ConclusionErythrocytic 5’-NT activity was more rapid and reliable to assess marginal Zn-deficient status in duck breeders. Marginal Zn deficiency impaired hatchability and antioxidant defense system and then induced the oxidative damage and apoptosis in embryonic liver, contributing to the greater loss of embryonic death.